High-altitude pulmonary edema: a clinical crisis

High-altitude pulmonary edema is a serious clinical condition observed in individuals participating in mountain climbing and skiing at high altitudes. High-altitude pulmonary edema is an oncardiogenic form of pulmonary edema. Atrial natriuretic factor and endothelin are implicated and ventilatory support is important in preventing fatalities.     

The correlation of the radiologic extent of lung transplantation edema with pulmonary oxygenation

OBJECTIVE: The study set out to evaluate the relationship between the efficiency of pulmonary oxygenation and the extent of the reimplantation response as revealed on chest radiography after bilateral lung transplantation. MATERIALS AND METHODS: Postoperative chest radiographs of 31 patients who had undergone bilateral lung transplantation were evaluated for the extent of the reimplantation response. For each patient, the contemporaneous oxygenation indexes (partial pressure of oxygen in arterial blood divided by fraction of inspired oxygen) were calculated and correlated with a radiographic score produced from the evaluation of chest radiographs. RESULTS: The method of evaluating chest radiographs for the extent of the reimplantation response was shown to be reproducible. Although mean oxygenation indexes were found to decrease with increasing radiographic scores, this trend was not statistically significant. CONCLUSION: Although the extent of the reimplantation response on the early postoperative chest radiography inversely correlated with the oxygenation efficiency of the transplanted lungs, this finding was not statistically significant.     

Postoperative acute pulmonary edema: a rare presentation of pheochromocytoma

The Duromedics bileaflet pyrolitic carbon mechanical prosthesis was introduced by Hemex in 1982 and subsequently acquired by Baxter. This communication documents a case of sudden leaflet fracture of a Duromedics mitral valve 48 months after implantation, which was managed successfully by replacement with a St. Jude Medical mechanical prosthesis. The patient presented in acute distress with paroxysmal atrial tachycardia and pulmonary edema. Transesophageal echocardiography was used to diagnose the leaflet fracture. The fracture had occurred transversely, with the fragments embolizing bilaterally to the iliofemoral arteries. These were removed at a subsequent operation. Cases of such fractures of the Duromedics prosthesis have been reported, with cavitation damage being the postulated mechanism.     

High-altitude pulmonary edema at a ski resort

MRI can accurately define the extension of cervical carcinoma to the parametria. However, in patients with cervical carcinoma clinical stage IB, the definition of the dimensions of the tumour, prior to surgery, and may also modify the treatment procedure. Recently pre-operative neoadjuvant chemotherapy has been proposed for patients with bulky tumours. Multiple factors may influence the prognosis of clinical stage IB and survival varies greatly among these patients. In particular the maximum dimensions of the tumour seem to have a prognostic relevance. The aim of this paper is to evaluate the potential of MRI to measure tumour size, in order to discriminate between patients needing surgery alone or pre-operative therapy followed by surgery. In 20 patients with clinical stage IB cervical carcinoma we performed MRI to measure the radius of the cervix, the radius of the tumour and their ratios. The measurements obtained have been compared with the corresponding data from histopathology of the operative specimens. The close correspondence between these linear measurements allows us to propose MRI as a reliable method to define tumour size in clinical stage IB patients before surgery.     

The correlation between symptomatic CMV infection and CMV antigenemia in heart allograft recipients

Previous studies have demonstrated that CMV-specific antigens detected from peripheral blood leukocytes correlate with active CMV infection in transplant patients. However, the clinical diagnosis of CMV infection is difficult, and the significance of a positive blood finding is unclear, while CMV antigenemia and viremia may also occur in asymptomatic patients. To investigate the clinical significance of CMV antigenemia after heart transplantation, 68 heart allograft recipients were monitored weekly. Altogether 501 blood specimens were analyzed. CMV was demonstrated in blood leukocytes by a monoclonal antibody and immunoperoxidase staining, and the antigenemia level was expressed as CMV positive cells/50,000 leukocytes. CMV antigenemia occurred in 28/68 patients, and 12 of them developed a symptomatic infection. Of all blood specimens 88/501 were CMV positive, and 30 of them related to the clinical manifestation of CMV. When antigenemia level exceeded > 100/50,000, a significant correlation between antigenemia and CMV-related clinical manifestation was reached (P < 0.001). Of the 28 antigenemia positive patients 16 never developed any clinical signs of CMV infection. Their maximal antigenemia level was low (median 23, range 30-90) compared with those with clinical manifestation (median 500, range 30-1000) (P < 0.002). In conclusion, high antigenemia levels (> 100/50,000) correlate with clinical manifestations of CMV infection. Patients with lower levels (< 100/50,000) do not necessarily ever develop a symptomatic infection. Quantitative monitoring of CMV antigenemia may, thus, be helpful in the clinical diagnosis of CMV infection in heart transplant patients.     

Cardiopulmonary baroreflexes: effects of pulmonary congestion and edema

Systemic vasodepressor reflexes were initiated in pump-oxygenator perfused dogs by separately pressurizing the pulmonary vessels and the left cardiac chambers. Pulmonary vascular pressurization caused transient systemic vasodilation of a magnitude proportional to stimulus pressure over the range 0-65 cmH2O. The sensitivity of this reflex was sigificantly less than that of the left heart baroreflex. Mild pulmonary edema produced by a period of sustained congestion, and moderate edema, caused by sustained congestion in the presence of alloxan, had no discernible effect on systemic vasomotor tone or on subsequent pulmonary vascular baroreflexes. By comparison of these results with earlier studies in similar preparations I concluded that pulmonary arterial baroreflexes could alone produce the response obtained by pressurizing the entire pulmonary vascular bed. Although it was anticipated that type-J, irritant, and stretch receptors would be affected by congestion, no systemic vascular effects attributable to them were seen.     

A lung ultrasound sign allowing bedside distinction between pulmonary edema and COPD: the comet-tail artifact

OBJECTIVE: Acute cardiogenic pulmonary edema and exacerbation of chronic obstructive pulmonary disease (COPD) can have a similar clinical presentation, and X-ray examination does not always solve the problem of differential diagnosis. The potential of lung ultrasound to distinguish these two disorders was assessed. DESIGN: Prospective clinical study. SETTING: The medical ICU of a university-affiliated teaching hospital. PATIENTS: We investigated 66 consecutive dyspneic patients: 40 with pulmonary edema and 26 with COPD. In addition, 80 patients without clinical and radiologic respiratory disorders were studied. MEASUREMENTS: The sign studied was the comet-tail artifact arising from the lung wall interface, multiple and bilaterally disseminated to the anterolateral chest wall. RESULTS: The feasibility was 100%. The length of the examination was always under 1 min. The described pattern was present in all 40 patients with pulmonary edema. It was absent in 24 of 26 cases of COPD as well as in 79 of 80 patients without respiratory disorders. The sign studied had a sensitivity of 100% and a specificity of 92% in the diagnosis of pulmonary edema when compared with COPD. CONCLUSIONS: With a described pattern present in 100% of the cases of pulmonary edema and absent in 92% of the cases of COPD and in 98.75% of the normal lungs, ultrasound detection of the comet-tail artifact arising from the lung-wall interface may help distinguish pulmonary edema from COPD.     

Arterial oxygenation and shunt fraction during one-lung ventilation: a comparison of isoflurane and sevoflurane

The aim of this study was to evaluate the effect of isoflurane and sevoflurane on oxygenation and shunt fraction during one-lung ventilation (OLV). Twenty patients undergoing lobectomy for lung cancer and scheduled for long-term OLV were enrolled in this study. Patients were allocated to treatment with either isoflurane or sevoflurane. Arterial oxygenation, shunt fraction, and hemodynamics were evaluated at the end of two-lung ventilation; 20 min after the initiation of OLV; 20 min after the application of 4-cm positive end-expiratory pressure (PEEP) to the dependent lung; 20 min after 8-cm PEEP; and 20 min after the conversion from OLV to two-lung ventilation. There was no significant difference between isoflurane and sevoflurane with regard to oxygenation, shunt fraction, or hemodynamics during OLV. PaO2 values after the application of 4-cm PEEP increased from 131.1 +/- 11.8 mm Hg to 190.6 +/- 22.9 mm Hg in the isoflurane group (P < 0.05) and from 127.2 +/- 14.3 mm Hg to 192.4 +/- 26.9 mm Hg in the sevoflurane group (P < 0.05). The selection of either isoflurane or sevoflurane for OLV was made without regard to arterial oxygenation and shunt fraction. PEEP application to the dependent lung is useful for improving oxygenation during OLV, but 8-cm PEEP had no added effect compared with 4-cm PEEP. Implications: We compared the effects of isoflurane and sevoflurane on oxygenation, hemodynamics, and shunt fraction during one-lung ventilation in 20 patients undergoing scheduled lobectomy for lung cancer. There was no significant difference between isoflurane and sevoflurane with regard to oxygenation, shunt fraction, and hemodynamics during one-lung ventilation. The application of 4-cm positive end-expiratory pressure increased the partial pressure of arterial oxygen during one-lung ventilation.     

Ozone-induced stimulation of pulmonary sympathetic fibers: a protective mechanism against edema

Tropospheric ozone exerts well-described toxic effects on the respiratory tract. Less documented, by contrast, is the ability of ozone to induce protective mechanisms against agents that are toxic to the lungs. In particular, interactions between ozone and the sympathetic nervous system have never been considered. Using a model of permeability edema in isolated perfused rabbit lungs, we report here that, immediately after exposure of rabbits to 0.4 ppm ozone for 4 hr, the pulmonary microvascular responses to acetylcholine and substance P are completely blocked. Several lines of evidence, including partial inhibition of the ozone-induced protective effect by several drugs (alpha2- and beta-adrenergic antagonists, neuropeptide Y antagonist, guanethidine), measured levels of released catecholamines in blood and urine and the in vitro response of isolated lungs exposed to 0.4 ppm ozone all seem to suggest that ozone can stimulate pulmonary adrenergic fibers and induce the local release of catecholamines and neuropeptide Y, this resulting in transient protection against pulmonary edema. We also showed that, 48 hr after the exposure, ozone increased the baseline microvascular permeability and the response to low concentrations of acetylcholine.     

Arterial blood gases in acute pulmonary edema

Arterial blood gas and pH measurements in 82 patients with acute pulmonary edema of cardiogenic origin entering the emergency department varied widely and were unpredictable using clinical examination. The mean arterial oxygen tension (PaO2) measured in 71 patients breathing room air was 59 mm Hg. Fourteen of the 82 patients were acidemic; 35, alkalemic and 33 had a pH in the normal range. The acidemic group had markedly lower PaO2, all under 60 mm Hg. Oxygen and furosemide were used in all cases and effectively corrected the hypoxia and reduced pulmonary congestion. Other drugs used included aminophylline (14 patients), morphine sulfate (9 patients) and digoxin (3 patients). Five of the nine patients who received morphine were hypercarbic initially but the CO2 retention did not worsen. No patient died during the initial 48 hours. This study reiterates the importance of directing therapy at ventilatory and cardiac abnormalities and points out the value of arterial blood gas monitoring to assess the initial status, monitor the patient's course, and to select drug therapy.     

Drug-induced pulmonary edema in a patient infected with human immunodeficiency virus

Adverse reactions to drugs are common in patients infected with the human immunodeficiency virus (HIV). In these patients pulmonary reactions to drugs may be difficult to differentiate from opportunistic pulmonary infections. We report a HIV-infected patient who on two occasions developed acute pulmonary edema related to the administration of ibuprofen.     

Sever acute pulmonary edema after peri-anesthetic laryngospasm in a newborn infant

Severe acute pulmonary oedema following peranaesthetic laryngospasm in a newborn. The authors report a case of severe acute pulmonary oedema secondary to a laryngeal spasm in a 3-week-old neonate, immediately after induction of anaesthesia with halothane. After emergency tracheal intubation, the infant experienced a severe, life-threatening pulmonary oedema requiring prolonged intensive care. Such a secondary time course is unusual. Usually pulmonary oedema has a favourable outcome after oxygen administration and maintenance of positive expiration pressure, except in the neonate.     

Neurogenic pulmonary edema in fatal and nonfatal head injuries

Impaired pulmonary function is a frequent but poorly understood complication of acute head injury (HI). A potential early contributor to the pulmonary dysfunction seen in HI patients is neurogenic pulmonary edema (NPE). We hypothesized that NPE would occur early after HI and that it would have a continuum of clinical severity depending on the severity of the HI and associated intracranial hypertension. A large autopsy data base and inpatient HI data base were used to search for cases of NPE. Patients in the autopsy data base were stratified according to injury type and whether they died at the scene or within 96 hours of injury. There were significant (p < 0.0001, analysis of variance) elevations in lung weights in patients dying at the scene and within 96 hours from HI, compared with those dying from other noncentral nervous system injuries. No other organs studied showed significant weight increases. The incidence of NPE in isolated HI patients dying at the scene was 32%. In patients with isolated HI dying within 96 hours, the incidence of NPE was 50%. We found an inverse correlation (r = 0.62; p < 0.0014) between the initial cerebral perfusion pressure and the PaO2/FIO2 ratio despite a normal-appearing chest x-ray film. We conclude that NPE occurs frequently in HI patients. The process of edema formation begins early in the clinical course and is isolated to the lung.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic and alveolar protein studies in noncardiac pulmonary edema

Hemodynamic data were obtained within 15 hours of admission in 11 previously healthy patients (20 to 51 years of age, 7 men and 4 women) who had developed transient, reversible pulmonary edema without cardiac dilation in association with near-death from freshwater drowning (2 cases), pentobarbital overdose, heroin overdose (2 cases), smoke inhalation, chest trauma, sepsis (2 cases), pancreatitis, or prolonged abdominal surgery with suspected sepsis. Using a balloon-tipped flow-directed catheter, the pulmonary artery systolic/diastolic pressures (in mm Hg) were 25/12, 22/9, 31/11, 26/15, 20/10, 35/15, 40/15, 32/18, 20/10, 24/10, and 20/7; the corresponding pulmonary capillary wedge pressures (in mm Hg) were 8, 9, 6, 14, 6, 6, 15, 15, 10, 10, and 5, respectively. Plasma colloidal osmotic pressures measured in the latter 5 cases were 26, 18, 18, 18, and 15 mm Hg, respectively. In addition, the protein content of the alveolar fluid was 5.1, 3.4, 4.0, and 7.1 g per 100 ml in 4 patients. The concentration and distribution of the protein in plasma and alveolar fluid were very similar. These findings provide strong efidence that altered capillary permeability is responsible for the pulmonary edema.     

Role of nitric oxide in sepsis-associated pulmonary edema

Transient pulmonary hypertension after inhibition of nitric oxide synthase (NOS) does not alter pulmonary reflection coefficients or lymph flows in endotoxemic sheep. To test the effects of persistent pulmonary hypertension induced by N omega-nitro-L-arginine methylester (L-NAME) and of inhaled NO on pulmonary edema, 18 sheep (three groups) were chronically instrumented with pulmonary artery catheters, femoral arterial fiberoptic thermistor catheters, and tracheostomy. The awake, spontaneously breathing animals received Salmonella typhi endotoxin (lipopolysaccharide; LPS) (10 ng/kg/ min) for 28 h. After 24 h, an airflow of 6 L/min was delivered through the tracheostomy. One group of animals (L-NAME/air) received L-NAME intravenously (25 mg/kg + 5 mg/kg/h) and breathed air. The second group (L-NAME/NO) was given L-NAME and NO (40 ppm) was added to the airflow. The third group was given NaCl 0.9% and breathed air (NaCl/air). Extravascular lung water was measured through the double-indicator dilution technique. Endotoxemia caused pulmonary edema, which was aggravated by L-NAME. Breathing of NO normalized pulmonary artery pressure (Ppa) and ameliorated pulmonary edema. Inhalation of NO may therefore be a therapeutic option for pulmonary edema associated with pulmonary hypertension.     

Monocrotaline model of noncardiogenic pulmonary edema in dogs

Monocrotaline, a plant alkaloid shown histologically to produce pulmonary endothelial damage and edema, was used in dogs to produce an acute model of noncardiogenic pulmonary edema. Following intravenous injection there was no change in pulmonary vascular pressures or heart rate; cardiac output fell and pulmonary vascular resistance increased. After 2 h measurement of lung water demonstrated modest pulmonary edema in all animals. The degree of edema produced was more consistent and reproducible than that following alloxan or alpha-naphthylthiourea.